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Biomedical subjects

C J Lockwood

Publications and source records attributed to C J Lockwood.

At least 109 records · Page 6Linked to original sources

Platelet disorders in pregnancy: implications for mother and fetus.

Platelet disorders in pregnancy are not uncommon. Most often, obstetricians are faced with a patient with undiagnosed thrombocytopenia and have the responsibility of deciding if the condition is ITP, gestational thrombocytopenia, or a process related to pre-eclampsia. Correct diagnosis is important because ITP can be associated with fetal thrombocytopenia, making route of delivery important. In alloimmune thrombocytopenia, the mother develops antibodies to a specific platelet antigen present on the fetal platelet but absent on her own. Severe AIT can cause intracranial hemorrhage and have disastrous consequences for the fetus and neonate. In preliminary studies antenatal intravenous gamma globulin therapy has shown promise in preventing the development of intracranial hemorrhage and ameliorating fetal thrombocytopenia. Essential thrombocythemia with a platelet count of greater than 600 x 10(9) platelet/L can occur in pregnancy; therapy consists of antiplatelet aggregating agents such as aspirin, and plateletpheresis. Platelet function disorders can be acquired or inherited. Acquired platelet dysfunction disorders are usually caused by drugs such as aspirin or indomethacin, or by a systemic disease. Hereditary disorders of platelet function can be diagnosed in utero, but cordocentesis may represent an unacceptably high risk. For prenatal diagnosis, other methods, such as chorionic villus sampling or amniocentesis, should be investigated as an alternative to the potentially high risk of cordocentesis.

Autoimmune Diseases↗

Retinal and pregnancy outcomes in the presence of diabetic proliferative retinopathy.

The objective of this study was to examine the retinal and pregnancy outcomes of pregnancies complicated by advanced diabetic retinopathy. Twenty pregnancies complicated by advanced diabetic retinopathy were included in this retrospective study. The data were analyzed to determine trends in perinatal outcome and to document the ophthalmologic performance. Ophthalmologic management included frequent funduscopic examinations by ophthalmologists of the Yale Retina Center. Among the 20 pregnancies, spontaneous abortion occurred in 2 (10%) and stillbirth in 1 (5%); the remaining 17 (85%) pregnancies culminated in live births at a mean gestational age of 36 weeks (+/- 2.3 SD), with a mean birth weight of 2,620 g (+/- 834 SD). The perinatal survival rate was 94%. Photocoagulation therapy was necessary prior to pregnancy in 45%, during pregnancy in 60% and postpartum in 65%. No pregnancies were terminated because of progressive visual changes that did not respond to photocoagulation therapy. Retinal status should not preclude pregnancy since contemporary methods of management can result in satisfactory retinal and pregnancy outcomes even in the presence of advanced diabetic microvascular disease.

Adult↗

Risk factors for severe preeclampsia.

OBJECTIVE: To identify risk factors associated with severe preeclampsia and to determine whether these factors are similar in nulliparous and multiparous patients. METHODS: Patients whose pregnancies were complicated by severe preeclampsia (n = 70) were compared retrospectively to 18,964 non-preeclamptic controls. Information on maternal demographic factors; medical, obstetric, and family histories; and neonatal outcome was retrieved and analyzed by univariate and multivariate analysis. RESULTS: By logistic regression, the only risk factors associated with the development of severe preeclampsia were severe obesity in all patients (adjusted odds ratio 3.5, 95% confidence interval [CI] 1.68-7.46) and a history of preeclampsia in multiparous patients (adjusted odds ratio 7.2, 95% CI 2.74-18.74). CONCLUSION: Severe obesity and a history of preeclampsia are the only maternal risk factors identified for the development of severe preeclampsia.

Adult↗

Recent advances in elucidating the pathogenesis of preterm delivery, the detection of patients at risk, and preventative therapies.

Preterm deliveries (PTDs) are a leading cause of neonatal morbidity and mortality in the world. Efforts to prevent PTD have been hampered by a poor understanding of the underlying pathophysiology, inadequate diagnostic tools, and generally ineffective therapies. There is increasing clinical and laboratory evidence that many PTDs result from premature activation of cells in the cervix, decidua, and fetal membranes in response to local mediators of maternal or fetal stress, ascending genital tract infection, and/or decidual hemorrhage. Putative mediators include peptide hormones (e.g. corticotropin releasing hormone (CRH)) and/or inflammatory-cytokines (e.g. interleukin-1, -6, and -8 (IL-1, -6 and -8)) which promote the production of oxytotic factors (e.g. prostanoids and endothelin) capable of eliciting uterine contractions and enhancing expression of proteases capable of initiating cervical change and/or membrane rupture. The identification of cervical, decidual, and/or chorionic extracellular matrix (ECM) proteins (e.g. collagen fragments and fetal fibronectin) and ECM-degrading proteases (e.g. collagenases and granulocyte elastase) in maternal serum and cervicovaginal secretions may provide new approaches to the detection of patients at high risk for PTD. In addition, our growing understanding of the pathogenic processes preceding PTD have led to new therapeutic approaches including antibiotic, anticytokine, and antiprotease treatments.

Anti-Bacterial Agents↗

Prenatal detection of monosomy 21 mosaicism.

We report a case of chromosomal mosaicism for monosomy 21 revealed in amniotic fluid cell culture. Ultrasound examination at 19 weeks' gestation showed in utero growth retardation and a complex cardiac malformation. A repeated amniocentesis confirmed the presence of monosomy 21 mosaicism. In view of the sonographically detected fetal abnormalities, termination of pregnancy was elected.

Abnormalities, Multiple↗

The presence of cervical and vaginal fetal fibronectin predicts preterm delivery in an inner-city obstetric population.

OBJECTIVE: It has previously been shown that fibronectin bearing a specific oncofetal domain is present at the chorionic-decidual interface and that its release into cervical and vaginal secretions accurately predicts preterm delivery in patients with uterine contractions. This study examines whether serial assessment of cervical and vaginal fetal fibronectin allows for the prediction of preterm delivery in symptom-free patients derived from an inner-city, general obstetric population. STUDY DESIGN: Cervical and vaginal samples were obtained from 429 consenting patients who received routine prenatal care between 24 and 37 weeks' gestation. A sensitive immunoassay was used to quantitate cervical and vaginal fetal fibronectin levels, and clinicians were blinded to fetal fibronectin results. Post hoc receiver operating characteristic curve analysis was used to determine which sample site (cervical or vaginal), fetal fibronectin concentration, and number of consecutive positive samples optimized screening efficacy. Logistic regression was employed to determine whether fetal fibronectin was an independent predictor of preterm delivery. RESULTS: The spontaneous preterm delivery rate was 11% (49/429). Among the 326 patients sampled within 28 days of delivery, receiver operating characteristic curve analysis indicated that the presence of a single cervical fetal fibronectin value > 60 ng/ml between 24 and 36 weeks' gestation predicted preterm delivery with a sensitivity of 73%, a specificity of 72%, and positive and negative predictive values of 25% and 95%, respectively. A vaginal fetal fibronectin value > 50 ng/ml predicted preterm delivery with a sensitivity of 68%, a specificity of 80%, and positive and negative predictive values of 30% and 95%, respectively. Cervical and vaginal fetal fibronectin predicted preterm deliveries resulting from both membrane rupture and preterm labor with intact membranes. A positive fetal fibronectin result preceded preterm delivery by 3.4 (+/- 3.2) weeks. Stepwise logistic regression demonstrated that cervical and vaginal fetal fibronectin levels were independent predictors of preterm delivery with adjusted odds ratios of 8.9 (95% confidence interval 3.6 to 22.1) and 6.0 (95% confidence interval 2.6 to 13.7), respectively. CONCLUSIONS: Among patients undergoing monthly cervical and vaginal sampling between 24 and 36 weeks' gestation, the presence of fetal fibronectin is a sensitive and specific predictor of preterm delivery.

Cervix Uteri↗

Double-blind; placebo-controlled trial of piperacillin prophylaxis in preterm membrane rupture.

OBJECTIVE: We attempted to test whether antibiotic therapy prolongs pregnancy in preterm premature rupture of membranes, because preterm premature rupture of membranes is frequently associated with chorionic-decidual infection. STUDY DESIGN: Women with preterm premature rupture of membranes and a singleton gestation at 24 to 34 completed weeks were randomized to receive either piperacillin 3 gm or placebo intravenously every 6 hours for 72 hours and were managed conservatively until spontaneous delivery, chorioamnionitis, or fetal distress. RESULTS: Between January 1987 and January 1992, a total of 75 patients were randomized to receive piperacillin (n = 38) or placebo (n = 37). There were no differences between the piperacillin group and the placebo group in mean gestational age at randomization (30.2 +/- 3 vs 30.3 +/- 2.9 weeks). However, a greater number of patients had pregnancy prolonged beyond 7 days (42.1% vs 10.8% p = 0.005) and the mean latency period was significantly prolonged (11.4 +/- 18.8 vs 6.1 +/- 13.6 days, p = 0.001) in the piperacillin group compared with the control groups. CONCLUSIONS: Use of intravenous piperacillin for 72 hours in preterm premature rupture of membranes significantly prolongs the latency period between membrane rupture and delivery.

Adult↗

The risk of second-trimester amniocentesis in twin gestations: a case-control study.

OBJECTIVE: Pregnancy outcomes in patients with twin pregnancy undergoing second-trimester amniocentesis for fetal karyotype assessment were compared in a case-control study with twin pregnancies undergoing routine ultrasonographic studies at similar gestational ages. STUDY DESIGN: All spontaneous and induced twin gestations that underwent ultrasonographic examination between 14 and 20 weeks were compiled for the period January 1987 through January 1992. Patients having undergone multifetal reduction or chorionic villous sampling and those with fetal anatomic or chromosomal anomalies, discordant growth (> 20%), death, or a monoamniotic sac detected at ultrasonography were excluded. RESULTS: The mean (+/- SD) maternal age was significantly higher among the 101 cases than among the 108 controls (35.2 +/- 3.5 vs 30.4 +/- 5.3 years, respectively; p < 0.01). No differences were noted in gravidity, parity, number of prior spontaneous losses, or gestational age at ultrasonography between the two groups. The fetal loss rate was similar among cases and controls (seven of 202 [3.5%] vs seven of 216 [3.2%], relative risk 1.07, 95% confidence intervals 0.3 to 3.5). No losses occurred within 3 weeks of the procedure. Gestational age at delivery, birth weight, mean Apgar scores at 1 and 5 minutes, and length of neonatal stay were not significantly different between cases and controls. CONCLUSIONS: Second-trimester amniocentesis in twin pregnancies is apparently not associated with excess pregnancy loss.

Abortion, Spontaneous↗

The effect of fetal gender on the prediction of Down syndrome by means of maternal serum alpha-fetoprotein and ultrasonographic parameters.

OBJECTIVE: Our investigation was designed to use maternal serum alpha-fetoprotein and individual or combinations of ultrasonographic parameters to examine the influence of fetal gender on the prediction of Down syndrome. STUDY DESIGN: A cohort study of 5114 patients who underwent karyotype analysis between 13 and 22 weeks' gestation was undertaken. Maternal demographic variables, anthropometric indices, and maternal serum alpha-fetoprotein values were assessed. Fetal parameters recorded included gender, biparietal diameter, head circumference, femoral and humeral length, transverse cerebellar diameter, and nuchal fold thickness. The effect of fetal gender on maternal serum alpha-fetoprotein values and ultrasonographic parameters was assessed. Gender-specific differences between fetuses with Down syndrome and euploid fetuses were identified, and the optimal cutoff values of individual and combinations of biometric parameters were determined by receiver operating characteristic curve analysis. RESULTS: A total of 42 fetuses with Down syndrome were identified. Female fetuses with Down syndrome had significantly lower maternal serum alpha-fetoprotein values than their male counterparts, and maternal serum alpha-fetoprotein screening paradigms resulted in the disproportionate identification of affected female fetuses. A nuchal fold thickness > or = 5 mm was the single best ultrasonographic predictor of Down syndrome independent of fetal gender. Affected male fetuses had significantly smaller mean femoral and humeral lengths than euploid fetuses after adjustment for biparietal diameter, but only the humeral length proved a clinically useful predictor of Down syndrome. Pearson's correlation coefficient confirmed that nuchal fold thickness and humeral length were independent of each other and of maternal age and maternal serum alpha-fetoprotein levels. The optimal ultrasonographic predictor of Down syndrome was the presence of either a nuchal fold thickness > or = 6 mm or a humeral length > 3.5 to 3.7 mm below the expected value. This combination of ultrasonographic findings identified 41.7% of female and 66.7% of male fetuses with Down syndrome. CONCLUSIONS: Fetal gender affects the prediction of Down syndrome by both maternal serum alpha-fetoprotein and ultrasonographic parameters. Moreover, the ultrasonographic detection of Down syndrome in fetuses is greatly improved by a combination of gender-specific biometric parameters.

Adult↗

Steroid regulation of oncofetal fibronectin expression in human cytotrophoblasts.

Oncofetal fibronectin (onfFN) is a uniquely glycosylated form of FN suggested to play a critical role in uterine/placental adherence during pregnancy. In the present study we have examined steroid regulation of onfFN in highly purified preparations (> or = 95%) of cytotrophoblasts isolated from human term placentas. Based on immunoassays, relative to controls, treatment of cytotrophoblasts with 10(-6) M medroxyprogesterone acetate (MPA) down-regulated media levels of onfFN 25, 53, 59, and 62% on days 1, 2, 3 and 4, respectively. The pattern of steroid regulation and levels of total FN were nearly identical to that of onfFN suggesting that chronic steroid treatment regulates synthesis of FN and not its oncofetal glycosylation. MPA treatment induced a 2-fold stimulation in media levels of hCG indicating that increased placental function was associated with steroid-mediated changes in FN expression. Steroid specificity experiments demonstrated that MPA, cortisol, and dexamethasone were potent inhibitors of onfFN expression whereas estradiol (E2), deoxycorticosterone, testosterone, progesterone, and the synthetic progestin OD-14, were not. This suggested that glucocorticoids and not progestins may be the physiologic regulators of placental FN expression and that MPA may mediate its matrix-modifying activity through a glucocorticoid-like mechanism. Treatment of cells with dexamethasone (10(-7) M) did not affect the levels of total protein synthesis or the release of human placental lactogen to the culture medium. This indicated that steroid-mediated down-regulation of onfFN expression in cytotrophoblasts did not result from a general reduction of protein synthesis. Based on densitometric scanning of Western blots, MPA and dexamethasone treatments down-regulated media levels of onfFN 70% relative to control levels. Northern blotting revealed that MPA and dexamethasone mediated a 60-90% reduction in steady state levels of FN mRNA in the presence or absence of E2. Our in vitro model may provide a unique system to evaluate steroidal effects on extracellular matrix (ECM) protein expression. In addition, we suggest that steroids may critically regulate placental ECM protein synthesis, and thus affect trophoblast/uterine adherence throughout pregnancy and expulsion of the placenta and membranes following delivery of the fetus.

Amino Acid Sequence↗

Complications of fetal blood sampling.

To examine the incidence and significance of complications related to percutaneous fetal blood sampling, we reviewed all the articles published in the English literature on this procedure. Risks of complications and adverse outcomes depend mainly on the gestational age at the time of the procedure, the operator's experience, and the indication for the procedure. To determine the incidence of fetal losses, we pooled the data from series with > 100 cases. After exclusion of cases where some fetal pathologic condition was present, we determined the incidence of adverse outcomes in a low-risk population. In this population fetal blood sampling performed by an experienced operator carries about a 1.4% risk of fetal loss before 28 weeks' gestation and a 1.4% risk of perinatal death (after 28 weeks).

Abruptio Placentae↗

Association between pregnancy-induced hypertension and asthma during pregnancy.

OBJECTIVE: Pregnancy-induced hypertension is an important cause of maternal mortality, intrauterine growth retardation, and perinatal mortality. We examined the relationship between pregnancy-induced hypertension and asthma. STUDY DESIGN: The study population consisted of 24,115 women without a history of chronic systemic hypertension who were delivered of live born and stillborn infants at Mount Sinai Medical Center between January 1987 and December 1991. Pregnancy-induced hypertension was defined as blood pressure of at least 140/90 mm Hg or an increase of > or = 30 mm Hg in systolic pressure or > or = 15 mm Hg in diastolic pressure. RESULTS: There was a significant association between pregnancy-induced hypertension and asthma during pregnancy (chi 2 = 17.86, p < 0.001). In addition, there was a significant upward trend in the incidence of asthma during pregnancy in women without, with moderate, and with severe pregnancy-induced hypertension (Mantel-Haenszel chi 2 = 11.8, p = 0.001). Logistic regression analysis demonstrated that the association between pregnancy-induced hypertension and asthma during pregnancy persisted after adjustment for the confounding factors of race or ethnicity, maternal age, parity, and prepregnancy weight (adjusted odds ratio 2.52, 95% confidence interval 1.47 to 4.35, p = 0.0008). An association between pregnancy-induced hypertension and a history of asthma was also found (chi 2 = 11.2, p = 0.001). However, after adjustment for potential confounders, this association failed to achieve statistical significance (adjusted odds ratio 1.2, 95% confidence interval 0.97 to 1.53, p = 0.083). CONCLUSION: Both pregnancy-induced hypertension and asthma might be caused by a third factor affecting smooth muscle reactivity.

Asthma↗

Is fetal blood sampling associated with increased beta-endorphin release into the fetal circulation?

This study was conducted to determine whether fetal blood sampling during the second trimester is associated with changes in circulating fetal beta-endorphin (BE) concentrations. We measured BE concentrations in 68 paired fetal and maternal blood samples obtained between 18 and 28 weeks' gestation. Patients were divided into a control group (n = 50), if the fetal blood samples were obtained by a single umbilical cord puncture, or multiple insertion group (n = 18), if multiple cord punctures were required to obtain a sample. The mean (+/- SE) fetal BE value for the multiple insertion group was significantly higher than BE levels from the control group (771.2 +/- 79.2 pg/ml versus 107.1 +/- 11.7 pg/ml; p < 0.001]. This elevation did not appear to be related to acidosis, since no differences in fetal umbilical pH were observed between the two groups. Fetal BE levels from the control but not from the multiple insertion group significantly correlated with maternal values (Spearman rank r = 0.59; p < 0.001 vs r = -0.08; p > 0.5). In neither group did fetal BE levels correlate with gestational age. These findings indicate that multiple cord punctures at the time of fetal blood sampling are associated with significant increases in BE release. Furthermore, although a maternal or placental contribution to steady state circulating fetal BE cannot be excluded, it would seem that the fetus itself is the primary source of elevated circulating BE levels following multiple cord punctures.

Cordocentesis↗

Glucocorticoid suppression of human placental fibronectin expression: implications in uterine-placental adherence.

Increased levels of glucocorticoids are associated with human parturition whether occurring before or at term. In the present study we examined the effects of glucocorticoids on placental fibronectin (FN) expression in cytotrophoblasts, isolated from human term placentas, to provide a potential mechanism through which glucocorticoids may influence uterine-placental adherence near parturition. Based on immunoassays, relative to controls, media levels of placental FNs bearing an oncofetal epitope (onfFN) were inhibited 65-80% by treatment with 10(-7) M dexamethasone (DEX) during experiments in which cumulative levels and daily release of onfFN were measured. DEX treatment increased human CG production by cytotrophoblasts approximately 3-fold without affecting the levels of total protein, suggesting that DEX treatment did not reduce placental function. DEX and cortisol inhibited onfFN expression with an EC50 of 2 and 16 nM, respectively. Other steroids were not effective in down-regulating onfFN expression, indicating that this was a glucocorticoid-specific response. In immunoprecipitation studies, treatment of cytotrophoblasts with 10(-7) M DEX for 3 days inhibited both release of labeled FN to the media and its incorporation into cell-associated material by approximately 80%. Results from Northern blotting indicated that DEX treatment suppressed levels of FN messenger RNA approximately 90% relative to controls. Levels of labeled laminin in media were inhibited approximately 80% by a 3-day treatment with 10(-7) M DEX, suggesting that glucocorticoids may coordinately suppress the synthesis of multiple extracellular matrix proteins in cytotrophoblasts. In our model, we propose that glucocorticoids may suppress placental extracellular matrix protein synthesis, which could lead to decreased uterine-placental adherence and be associated with parturition.

Blotting, Northern↗

Progestational regulation of human endometrial stromal cell tissue factor expression during decidualization.

Decidualized endometrial stromal cells from mid- to late secretory phase and decidual cells from gestational human endometrium displayed prominent immunohistochemical staining for tissue factor, a primary initiator of hemostasis. Consistent with the regulation by progesterone of the decidualization process in vivo, medroxy-progesterone acetate elevated the tissue factor content of primary stromal cell cultures 8-fold over basal values. This increase paralleled the release of immunoreactive PRL, a marker of decidualization. The induced, as well as basal, tissue factor displayed full functional activity and the expected electrophoretic mobility (46 kilodaltons). Moreover, Northern analysis of RNA from cultured stromal cells indicated that medroxyprogesterone acetate increased tissue factor mRNA levels approximately 10-fold relative to control levels. In contrast, cultured stromal cell tissue factor protein content and mRNA levels were unaffected by exogenous estradiol. These findings indicate that enhancement of endometrial stromal cell tissue factor content is associated with progesterone induction of the decidualization process. In humans, trophoblastic invasion of the endometrial vasculature during blastocyst implantation risks hemorrhage. Therefore, increases in perivascular decidual cell tissue factor expression could serve to promote periimplantational endometrial hemostasis.

Blotting, Northern↗

Progestin regulation of plasminogen activator inhibitor type 1 in primary cultures of endometrial stromal and decidual cells.

The progestin medroxyprogesterone acetate (MPA) enhanced expression of the endothelial-type plasminogen activator inhibitor PAI-1 by stromal cells from cycling endometrium and by decidual cells from first trimester endometrium. In the cultured stromal cells, Northern analysis revealed a 4-fold increase in steady state levels of PAI-1 mRNA in response to 10(-6)-10(-8) mol/L MPA. Although the cells were refractory to 10(-8) mol/L estradiol (E2) alone, E2 plus MPA produced a further doubling of PAI-1 mRNA levels. Parallel effects on PAI-1 protein levels in the stromal cell-conditioned medium were measured by immunoassay and confirmed by immunoblot analysis. During an initial 3-day exposure, PAI-1 levels were elevated 6- and 12-fold by MPA and E2 plus MPA, respectively, compared with those in either control or E2-treated cells. In the subsequent 3 days of culture, PAI-1 levels were increased 30-fold by MPA and 70-fold by E2 plus MPA. Cultured decidual cells released significant quantities of PAI-1 under basal conditions; these levels were also elevated by MPA and increased markedly by E2 plus MPA. While PAI-2 was also detected in both stromal and decidual cell cultures, its levels were far lower than those of PAI-1 and were unaffected by exogenous steroids. Extrapolation of these in vitro results to periimplantational events in humans suggests that under progesterone regulation, decidual cell-derived PAI-1 could 1) restrain blastocyst invasion of the stroma by inhibiting trophoblast-associated urokinase-type plasminogen activator, and 2) prevent hemorrhage during trophoblast invasion of the endometrial vasculature by inhibiting fibrinolysis mediated by tissue-type plasminogen activator.

Blotting, Northern↗

Steroid-modulated stromal cell tissue factor expression: a model for the regulation of endometrial hemostasis and menstruation.

This study examined steroidal regulation of tissue factor expression by cultured endometrial stromal cells. Confluent stromal cell cultures derived from cycling human endometria were exposed to vehicle control, 10(-8) mol/L estradiol (E2), 10(-8)-10(-6) mol/L medroxyprogesterone acetate (MPA), or both E2 and MPA for 2-24 days in serum-containing medium. The progestin enhanced immunoreactive and functionally active stromal cell tissue factor content, achieving peak effects by 8-12 days of culture. Although E2 alone was ineffective, it augmented MPA-enhanced tissue factor content by 8 days of culture, with continued increases beyond 20 days. Dose-dependent effects on tissue factor protein content were observed between 10(-8)-10(-6) mol/L MPA added alone or together with E2. The content of tissue factor mRNA was also increased by MPA and synergistically increased by E2 plus MPA. Similar steroidal effects on stromal cell tissue factor protein and mRNA content were observed using a defined medium. After optimal induction of tissue factor expression by E2 plus MPA, removal of these steroids reduced levels of stromal cell tissue factor mRNA and protein, with virtually complete reversal by day 7 of withdrawal. These time-course and dose-response relationships establish in vitro conditions with which to dissect factors controlling endometrial hemostasis, whereas the observed effects of steroid withdrawal establish a novel model for the study of mechanisms regulating normal and abnormal uterine bleeding.

Cells, Cultured↗

New approaches to the prediction of preterm delivery.

Current approaches to the detection of patients at risk for preterm delivery (PTD) have focused on the diagnosis of preterm labor. However, these approaches are complicated by treatment biases and our inability to convincingly differentiate preterm labor from Braxton-Hicks contractions. Moreover, preterm labor with intact membranes accounts for only one-half of all spontaneous PTDs since uterine contractions follow preterm premature rupture of the membranes (PROM) in an additional 50% of cases. Clinical dogma holds that the prevention of PTD requires the early detection of at risk patients. However, clinical indicators of PTD risk including cervical change, uterine contractions, vaginal bleeding, maternal demographic featuers and obstetrical history have poor sensitivity and/or specificity. Fortunately, an improved understanding of the association between preterm parturition and cervical, chorionic and decidual extracellular matrix degradation has led to a number of promising new biochemical indices of the proteolytic processes leading to PTD. These include measurement of serum collagenase activity and assessment of cervico-vaginal granulocyte elastase and oncofetal fibronectin levels. It remains to be seen, however, whether an improved detection of patients at risk will lead to a reduction in the occurrence of PTD.

Cervix Uteri↗